By behavioral analysis (movement-notation of films) and neurophysiological measures (EEG and EMG) of the somnolence, catalepsy, and akinesia produced by lateral hypothalamic damage or by drugs in rats and cats, we have demonstrated: (1) independent motor subsystems (support, locomotion, head scanning, orienting and mouthing) that are involved in all motivated behavior, but have not been analyzed adequately previously. Selective suppression or exaggerated dominance of particular combinations of these subsystems may account for many of the "bizarre" behaviors seen in catalepsy and akinesia. (2) New sources of spontaneity in motivated behavior: (a) positive reafferent activation ("warm-up") provides a source of tonic activation and increased amplitude of movement in recovering akinetic rats. (b) Contact with the ground or water provides "spontaneity" in rats with combined midbrain lesions. These animal models will be useful experimental analogs for some of the symptoms of Parkinson's disease. (3) Morphine catalepsy is entirely different from catecholamine-depletion catalepsy, involving different motor subsystems and different forms of rigidity. We are continuing our analysis of these subsystems in normal and brain damaged animals. In addition, the state of somnolence induced by lesions versus that induced by morphine is being analyzed.